Inflammation and Apoptosis-Related Damage in Lung, Liver, and Kidney Tissues due to Subarachnoidal Hemorrhage

Objective: Oxidant and inflammatory substances released into the blood due to subarachnoidal hemorrhage (SAH) can pass into the peripheral compartment, causing distant organ damage due to blood-brain barrier permeability caused by oxidative stress, inflammation, and apoptosis. This study aimed to demonstrate the secondary damage to peripheral organs, including the lung, kidney, and liver, resulting from SAH. Material and Method: Twenty rats were divided into sham and SAH groups, each consisting of ten animals. In the SAH group animals, 0.3 mL autologous blood taken from the tail artery was injected into the cisterna magna for 2 minutes. Seven days after SAH formation, all animals were euthanized under anesthesia. Following decapitation, brain tissues, lung, liver, and kidney tissues were placed in 10% formaldehyde for histopathological and immunohistochemical analysis. Results: In the SAH group, neuronal degeneration in the cerebral cortex, and hyperemia and hemorrhage in the lung, kidney, and liver were observed histopathologically. In immunohistochemical examinations, decreased expression of brain-derived neurotrophic factor (BDNF) and neurofilament (NF) in the cerebral cortex, cerebellum, and hippocampus sections; In lung tissues, enhanced caspase (Cas)-3, hypoxia-inducible factor 1 alpha (Hif-1α) and nuclear factor kappa beta (NF-κB) expressions in the lung, Cas-5, cyclooxygenase-1 (Cox-1) and interleukin (IL)-1 expressions in the liver, Cas-3, Cox-1 and IL-3 expressions in the kidney were observed. Conclusion: Following SAH, in addition to damage to brain tissue, peripheral tissues such as the lung, kidney, and liver can also be damaged through inflammation and apoptosis.